Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018991 (hemiplegia)
 3,997 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study cerebral metabolism in neonates after unilateral cerebral infarcts 4 neonates (3 full-terms, one preterm with a gestational age of 35 weeks) with unilateral cerebral infarcts were examined at 7 to 49 days of postnatal age, using proton magnetic resonance spectroscopic imaging (1H-MRSI). Three neonates had infarcts of the left middle cerebral artery (MCA), one had a right posterior cerebral artery infarct and a more localized anterior lesion. Examinations were repeated in the three fullterm infants aged 2-3 months. Lactate resonances, which are not present in normal brain after term age, were demonstrated in two patients tested at 7 and 10 days of age respectively, and in one of them lactate was still present at two months. In all four neonates a decrease of the N-acetylaspartate/choline (NAA/Cho) ratio was seen within the area of infarction. Repeated MRS of two infants at three months showed an increase in NAA/Cho ratios in all brain areas, but values remained below normal in the infarcts. In the third infant a further decrease in the NAA/Cho ratio was demonstrated in the area of infarction at two months. The NAA/Cho ratios in the surrounding and contralateral brain tissue were normal in all infants. All three infants with a MCA infarct developed a hemiplegia. The aforementioned metabolic alterations in neonates with cerebral infarcts, demonstrated using 1H-MRSI, were found to be confined to the area of infarction and abnormalities persisted beyond the neonatal period.
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PMID:Proton magnetic resonance spectroscopic imaging in neonatal stroke. 883 79

A case of cerebral infarction with transient cerebral arteriopathy in a 12-year-old female is described. The child showed with an acute onset of left hemiplegia, central facial palsy and aphasia. She was diagnosed with right internal carotid artery obstruction with no predisposing factors for cerebral infarction. A serial MR image and MR spectroscopy of the brain was performed. MR angiography revealed reversible vascular changes in the right middle cerebral artery after several months. The ratio of choline/creatine was elevated and that of N-acetylaspartate (NAA)/creatine was depressed in the cerebral lesion, however, they were normalized during the remission phase with long echo time-MR spectroscopy. The elevation of the lactate peak was clarified with short echo time-MR spectroscopy. The longitudinal follow up using MR angiography, and MR spectroscopy with long and short echo time was useful for the evaluation of reversible vascular change with cerebral infarction in children.
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PMID:MR imaging and 1H-MR spectroscopy in a case of cerebral infarction with transient cerebral arteriopathy. 1553 56

Familial hemiplegic migraine type 2 (FHM2) is an autosomal dominant inheritance disorder caused by ATP1A2 mutation, and the clinical spectrum is heterogeneous even with acute severe encephalopathy. However, up to now, early treatments against acute and severe attacks in FHM2 are still insufficient. Here, we report a 15-year-old female with intellectual disability due to FHM2 caused by a pathogenic ATP1A2 gene mutation, presenting mild-to-moderate headache at the onset, followed by confusion, complete right hemiparalysis, epileptic partial seizures, and conscious disturbance with rapid progression in acute attack. Brain magnetic resonance imaging (MRI) and magnetic resonance spectroscopy have revealed left extensive cerebral cortex edema, slightly decreased N-acetylaspartate for neuronal damage, and mildly increased lactate acid for mitochondrial dysfunction throughout the hemispheric swollen cortex. The patient is diagnosed as severe encephalopathy caused by FHM2. Based on literature review about pathophysiologic mechanism described in FHM2 recently, we use early treatments including prevention of glutamatergic excitotoxicity and protection of mitochondria function, as well as traditional antimigraine drug. The symptoms are all greatly improved and recovered within a short time, and follow-up MRI also shows complete disappearance of edema throughout the left hemispheric cortex. Altogether, the approach in our case may reduce the severity and duration of encephalopathy effectively, expend therapeutic options, and provide helpful references for acute severe encephalopathy in FHM2.
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PMID:Early Treatment in Acute Severe Encephalopathy Caused by ATP1A2 Mutation of Familial Hemiplegic Migraine Type 2: Case Report and Literature Review. 3176 58